Structure of viral RNAs: (1) The analytical complexity of avian and murine tumor virus RNAs. (2) Physical and chemical differences between the RNAs of nondefective RNA tumor viruses and those of replication-defective and transformation-defective deletion mutants. (3) Specific sequences of 30-40S tumor virus RNAs will be mapped physically relative to the poly(A) terminus of the RNA. Such sequences will be identified by the unique RNase T1-resistant oligonucleotides they contain. Some of these sequences will be functionally identified, by correlating their absence from deletion mutants with the known functional defects of these mutants. This should provide a gene order of tumor virus RNAs. (4) Evidence for possible host-modification of viral RNA is being sought for. (5) The messenger function of intracellular viral RNA species (30-40S and 20-30S) will be investigated. (6) The mechanism of crossing-over among RNA tumor viruses will be studied from the several aspects: (a) Physical maps of RNase T1-resistant oligonucleotides of viral recombinants and their parents will be compared to those of their parents, to determine the number of cross-over points. (b) Evidence for the presence of heterozygotes, postulated to be intermediates in recombination, will be looked for. (7) The generation of deletion mutants is being investigated: mapping deleted sequences on wild-type RNA is exected to indicate the map location of the deleted function in the wild-type genome and to explain whether deletions were from the end (perhaps caused by incomplete transcription) or from within (likely to occur at the level of proviral DNA) the wild-type RNA. (8) The study of the chemical and genetic relationship between the two major RNA components of murine-leukemia sarcoma viruses is proposed by RNA-DNA hybridization and comparative fingerprint and mapping analyzes of RNase T1-resistant RNAs. The present state of this field provides evidence ranging from very close to very distant relationships between the two RNA components.